234 PSYCHOLOGICAL EFFECTS OF ALCOHOL. 



Practically it might make no difference whether a given acceleration 

 was produced by one mechanism or the other; but for the theory of the 

 effect of alcohol on neuro-muscular tissue it is of the utmost importance 

 whether or not the autonomic system reacts in a directly opposite way 

 to that of the cerebro-spinal. For theoretical reasons we are under 

 obligations to ask the bearing of our data on the question whether the 

 pulse-acceleration as effected by alcohol is due to a positive stimulation 

 of the cardiac accelerator or to a partial paralysis of the cardiac in- 

 hibiting mechanism. 



In the conflicting answers of traditional experiments to the funda- 

 mental direction of the effect of alcohol on the human pulse, it is not 

 surprising that there is scant experimental evidence with respect to 

 the origin of that effect. Dixon, 1 Reid Hunt, 2 and Lauder Brimton 3 

 hold that in view of the reflex acceleration of the heart from the stimu- 

 lation of various afferent nerves, the acceleration of the heart by alcohol 

 is a reflex of the vasomotor center to the local irritation of the mouth 

 and stomach. But apparently the evidence for this view is indirect 

 rather than direct. Our own data can not be harmonized with this 

 hypothesis. If the relative acceleration were a reflex to local irritation, 

 it should be most pronounced soon after the ingestion of alcohol, and 

 should gradually decrease as the alcohol is absorbed. Our association 

 data, on the contrary, show a relatively small effect in the first half 

 hour and a gradually increasing relative acceleration up to the end of 

 the 3-hour experimental session, when the alcohol by absorption and 

 dilution may be supposed to have lost a large part or all of its effect on 

 the stomach-walls as a local irritant. 



Hascovec 4 found with dogs that atropin, which specifically paralyzes 

 the vagus endings in the heart, increases heart-rate after alcohol. But 

 even that, if it were conclusively demonstrated for humans, would 

 hardly answer our question. 



The observations of Reid Hunt 2 on the differential effect of accel- 

 erator and inhibitor mechanisms on the relative length of systole and 

 diastole give us the only non-operative technique which is commonly 

 accepted as proving the involvement of either of the two heart-regu- 

 lating systems. Hunt found that after stimulating the accelerator 

 both diastole and systole decrease together, while as a result of the loss 

 of vagus tone the chief loss is in diastole. In this manner he proved 

 that chloral, chloroform, and ether affect chiefly the cardio-inhibitory 

 center, and seem to have but little effect on the accelerator center. 

 The chief difficulty in applying the method of Hunt to ordinary sphyg- 

 mograms is the indistinctness and uncertainty of the separation between 

 systole and diastole, which is incident to the interaction of the natural 



'Dixon, Journ. Physiol., 1907, 35, p. 346. 



2 Hunt, Am. Journ. Physiol., 1899, 2, p. 395. 



3 Brunton, Therapeutics of the Circulation, London, 1914, p. 17,s. 



^Hascovec, Wiener med. Wchnsch., 1909, 59, p. 457. 



